Document 58967

Brown Recluse Spider Bites
Thomas P. Forks, DO, PhD
Background: Brown recluse spider bites are a serious medical problem in the southeastern United
States. Although most bites are asymptomatic, envenomation can result in a constellation of systemic
symptoms referred to as loxoscelism. Patients can also develop necrotic skin ulcers (necrotic arachnidism). These ulcers are often difficult to heal and can require skin grafting or amputation of the bitten
Metbods: Asearch of the literature was performed using the search words "spider envenomation,"
"brown recluse spider bites," and "arachnid envenomation."
Results and Conclusions: Most brown recluse spider bites are asymptomatic. All bites should be
thoroughly cleansed and tetanus status updated as needed. Patients who develop systemic symptoms
require hospitalization. Surgical excision of skin lesions is indicated only for lesions that have stabilized and are no longer enlarging. Steroids are indicated in bites that are associated with severe skin
lesions, loxoscelism, and in small children. Dapsone should be used only in adult patients who experience necrotic arachnidism and who have been screened for glucose-6-phosphate dehydrogenase deficiency. Topical nitroglycerin can be of value in decreasing the enlargement of necrotic skin ulcers.
(J Am Board Fam Pract 2000;13:415-23.)
Brown recluse spider bites are a relatively common
problem in the United States and occur most frequently in the midwest, south-central and southeastern areas of the country. According to the Centers for Disease Control, these bites are not a
reportable illness; consequently, the numbers of
patients developing systemic or cutaneous manifestations caused by the venom of these spiders can
only be guessed. 1 These bites can result in considerable morbidity and occasionally require the amputation of an involved extremity. Deaths from
spider bite, although rare, are usually caused by the
induction of renal failure as a consequence of red
blood cell hemolysis. Treatment of these bites is
controversial and is generally directed at managing
the cosmetic injury to the integument. A secondary
focus of treatment is the management of the less
frequent but potentially more serious systemic effects of the neurotoxic venom, often referred to as
loxoscelism. Gangrenous spot, or necrotic spot of
Chile (dermonecrosis), as a consequence of the bite
Submitted, revised, 16 February 2000.
From the Department of Family Medicine, The University of Mississippi Medical Center, Jackson. Address reprint
requests to Thomas P. Forks, DO, PhD, Department of
Family Medicine, The University of Mississippi Medical
Center, 2500 North State Street, Jackson, MS 39216-4505.
of the venomous South American brown spider
(Loxosceles Ioeta) was initially described by Macchiavello in 1937.2 It was not until 1957 that investigation by Atkins et al 3 implicated venom of the brown
recluse spider (Loxosceles reclusa) as the agent of
necrotic arachnidism in the United States.
A search of the literature was performed using the
search words "spider envenomation," "brown recluse spider bites," and "arachnid envenomation."
Brown Recluse Spider
All spiders are poisonous; however, most have fangs
that are too small to penetrate the skin of human
beings. There are 23 or 24 genera, including 60
odd species of spiders indigenous to the United
States, that have been implicated in causing human
injury. Members of at least six of these genera
produce bites that can be confused with those of the
brown recluse spider. These genera (AtrtlX, Argiope,
ChirtlCanthium, Lycosa, Phidippus, Tegenaria) include
the wolf, jumping and yellow garden spiders. These
spiders are common, well recognized inhabitants of
neighborhood backyards and flower gardens. The
hobo spider (Tegenaria agrestis) has recently been
implicated in cases of necrotic arachnidism in the
Brown Recluse Spider Bites 415
northwest United States. 1,4 Members of Atrar are
not indigenous to the United States. Members of
this genus are normally found in eastern Australia
and inflict human bites in the United States when
imported with Australian produce. Worldwide,
there are at least 200 species of spiders that have
been implicated in the cutaneous or systemic poisoning of human beings. 5
Numerous other indigenous North American
insects and animals, including kissing bugs, ticks,
scorpions, bedbugs, biting flies, fleas, snakes, rats,
and mice, produce bites that can be superficially
confused with mild cases of loxoscelism.6 Other
disease states, including herpetic ulcers, burns,
trauma, diabetic ulcers, rhus dermatitis, bed sores,
pyoderma gangrenosum, Stevens-Johnson syndrome, erythema nodosum, drug reactions, thromboangiitis obliterans, and vascular disease,'-9 also
produce skin lesions that can be confused with cases
of necrotic arachnidism. Consequently, unless the
offending animal is presented for identification
with the bitten patient, it is prudent to designate all
suspected brown recluse spider bites as presumptive brown spider bites, or presumptive necrotic
arachnidism until definitive proof is obtained.
Six-eyed spiders (family Loxoscelidae) are represented in the United States by 13 species of
spiders. Five of these species (L IlrizoniclI, L reciuslI,
L rufescens, L desertll, and L laeta) have been implicated in systemic poisoning of bitten patients.
These species are all very similar and all five species
are appropriately referred to as fiddleback or violin
spiders. Although there is some interspecies variation in potency, all Loxosceles species produce a
neurotoxic venom that can potentially induce dermonecrosis, varied systemic symptoms, and anaphylaxis in bitten patients. Loxosceles species are
found in all the states as a result of translocation on
clothing, bagging, and camping gear. Intrastate and
interstate relocation of home furnishings and belongings, along with the nests, spiders, and eggs
contained therein, is also involved in the movement
of these spiders into nonindigenous areas.
The brown recluse spider (brown spider, recluse
spider) is the most widely distributed member of
the genus in the United States and is the species
most often implicated in necrotic arachnidism. L
reciuslI is indigenous to the states roughly south of
the Mason-Dixon line or approximately 42 degrees
latitude and east of 100 degrees longitude. These
spiders can be found eastward from the western
November-December 2000 Vol. 13 No. 6
borders of Texas, Oklahoma, and Kansas to the
Atlantic coast. Isolated populations of this species
can also be found in the more northern states of
Nebraska, Iowa, Illinois and Ohio. The species is
most concentrated in the central plain states of
Arkansas, Kansas, Oklahoma, and Missouri. Specimens have also been identified from California and
Hawaii after presumably being transported to those
locations with the personal possessions of travelers.
L IlrizoniclI is indigenous to Arizona, New Mexico, Nevada, Texas, Utah, southern California, and
northwestern Mexico; serious complications secondary to envenomation by this species have also
been documented. lo L desertll, also known as L
unicolor, is relatively uniform in color and its violin
is nearly indistinct. This species has been less well
studied and is normally found in the deserts of the
western states. In the United States, L rufescens is
most commonly found in Texas and is referred to
by Gertsch ll as a cosmopolitan species, ie, a species
introduced into the United States from Central
America on commercial vehicles.
Envenomations by L rufescens and L laeta are
well documented from Central and South America. 12 L rufipes and L gllucho are also medically
important species in Central and South America,
respectively. Loxosceles species is represented in Africa by 17 species, and reports of bites on the
African continent (L rufescens, L parnl1m) have been
published in the literature. 13 Envenomations from
Loxosceles species have also been reported from Europe and the Mideast, including Israel, presumably
by L rufescens. 14 Southcott15 documented bites
from the Australian continent (L rufescens, L laeta).
Envenomations have also been repqrted by unknown species (probably L rufoscens) from China,
Russia, and Japan.
Natural History
Brown recluse spiders are generally shy and inoffensive. These spiders invariably seek shelter in
abandoned or infrequently used buildings, in basements, under tables, in dresser drawers, or in stairwells. They can also be found in stored clothing,
under wood or rock piles, and within the loosened
and flaking bark of trees and logs. They produce
small, irregularly formed webs (sheets) that cover
and line their burrows or hides. These nocturnal
spiders prey on various small invertebrates and insects, including firebrats and related silverfish. 16
Although they have been shown to live up to 3
years in reproduced, artificial environments, their
natural life span is probably about 1 year.
Morphologically, female brown recluse spiders
are slightly larger than the males and average 9 mm
in length. Older, mature spiders are capable of
attaining lengths up to 3 or 4 cm, inclusive of their
legs. The body accounts for approximately one fifth
of the adult size and is light tannish brown or
gray-brown in color. Female brown recluse spiders
are generally larger than the males; consequently,
they produce a larger amount of venom and their
bite is potentially more serious. The distinctive,
dark brown or black violin, from which the spider
receives its name, is situated on the dorsal aspect of
the oval cephalothorax. Individual spiders commonly darken as they age, and the violin can become indistinguishable. The neck of the violin is
oriented toward the grayish, oblong, sensillumcovered abdomen of the spider.
In contrast to most spider species, recluse spiders possess six eyes arranged in a semicircle of
three diads rather the eight eyes of other species.
Adult spiders can live approximately 6 months
without eating and can withstand temperature extremes of 8° to 43° cY Their ability to tolerate
such variations in temperature contributes to their
survival when accidentally transported to extreme
or unusual environments, eg, Finland. Researchers
discovered that the entire first floor of a University
of Helsinki building was infested with imported L
laeta. 18
Fiddleback Venom
The collection of adequate volumes of brown recluse venom for biochemical analysis has been difficult and challenging. Researchers have attempted
to collect and fractionate venom for study by using
electrical stimulation and microdissection of the
venom glands. These studies have indicated that
the hemolytic component of the venom is heat
labile, calcium dependent, and optimally active at a
pH of 7.1. Collectively, research to date has shown
that purified brown recluse venom contains a minimum of eight or nine different enzymes and proteins, including alkaline phosphatase, esterase,
lipase, protease, hyaluronidase, hemolysins, levarterenol bitartrate, and sphingomyelinase D.
Sphingomyelinase D is the most important and
most active enzyme in brown recluse spider venom.
VMOIII PlllbopbysIoloD
Electron microscopic studies of rabbit blood vessels
have shown endothelial damage as soon as 3 hours
after the manual injection of brown recluse venom.
This damage is accompanied by thrombocytopenia,
altered prothrombin and partial thromboplastin
times, and decreased fibrinogen levels. Shortly
thereafter, small capillaries become occluded with
thrombi, resulting in further tissue anoxia and destruction. 19 Anderson20 indicated that large quantities of platelets become trapped very early in venom-damaged capillaries. Tissue necrosis is grossly
visible at 24 hours after envenomation.
Studies investigating the hemolytic activity of
brown recluse venom have produced conflicting
results. Material extracted from the cephalothorax
of brown recluse spiders has been shown to induce
the direct hemolysis of human red blood cells. 21
Cephalothorax extracts contain materials from
both the gut and venom glands of spiders. In their
1966 case report, Taylor and Dennr2 described
the clinical course and death of a man who was
presumed to have been bitten by a brown recluse
spider and who developed hemolysis and renal failure. Smith and Micks23 were unable to elicit any
hemolytic activity of the venom of L laeta, L rec/us(l,
and L rufescens. Abdominal extracts, however
caused the in vitro hemolysis of human red cells.
Morgan et al 24 reported the in vitro hemolysis of
human red blood cells in blood plasma when brown
recluse venom was added. Chu et al25 described the
case of a 2-year-old boy who was bitten on the
chest and who developed a severe case of hemolytic
anemia. This patient did not develop a corresponding dermonecrosis. Futrell et al26 proved that a very
active component of brown recluse venom attaches
to human red cell membranes. They speculated
that the resulting lysis of the red blood cells was
accomplished through an interaction between this
component and complement factors contained in
human serum. Conclusive evidence of the lytic activity of brown recluse venom on human red blood
cells was described by Forrester et al. 27 Wtlliams
and coworkers28 described two cases of severe hemolytic anemia resulting from brown recluse envenomation. One adult female patient suffered a
fatal myocardial infarction after debridement of the
large necrotic ulcer on her right upper arm.
Morgan and Felton29 illustrated human epithelial cell breakdown secondary to brown recluse
venom. A generalized breakdown of body fats in
Brown Recluse Spider Bites 417
insects has been shown to occur by Eskafi and
Nonneneo after injection of brown recluse venom.
Sphingomyelinase D is a major component of
brown recluse spider venom and has been shown to
be cytotoxic to both endothelial cells and red blood
cells. 27 This enzyme has also been shown to induce
tissue necrosis in rabbit tissue. 31 •32 Tissue necrosis
is directly attributable to the induction of endothelial cell disruption, intravascular hemolysis, platelet
aggregation, and thrombi fonnation by sphingomyelinase D. This enzyme is also implicated in the
disruption of nerve impulse transmission and in
contributing to cutaneous anesthesia. 33 Tissue necrosis is also partly due to polymorphonuclearleukocyte-induced vasculitis.
The hyaluronidase in the venom contributes to
the fluidity of the tissue and resultant spread of
venom through the subcutaneous tissue. Gravity
might play some role in the spread of the venom
and degraded tissue into dependent tissues. Bites in
fatty areas seem to fare worse. It has been postulated 20 that the lipase and other components of the
venom act directly on the fatty tissue, releasing
small microemboli and nonphysiologic products
into the bloodstream.
Clinical Presentation
When initially bitten by brown recluse spiders,
many patients experience a mild burning sensation
that might resolve only to reoccur much amplified
several hours later. Pruritus, pain, and erythema
can develop around the bite site during the first 6
hours after the bite. Hobbs and Harre1l 34 described
the fonnation of an ischemic ring, followed by the
development of an irregular erythematous ring surrounding the bite site within the first 24 hours.
Some patients, presumably those who have experienced minimal envenomation, are devoid of any
discomfort at the time of the bite and are mystified
at the subsequent emergence and evolution of skin
lesions. Patients are usually bitten when they are
dressing themselves by spiders that have previously
crawled into their clothing. When bites are immediately painful, the spiders are invariably crushed.
All spiders should be brought in by the patient for
proper identification even if only partial remains
can be collected. Using a hand lens or other suitable magnifying device, the physician might be able
to identify the diagnostic six eyes of the spider,
thereby making the diagnosis of loxoscelism cer-
418 JABFP November-December 2000 Vol. 13 No. 6
Table 1. Systemic and Cutaneous Symptoms of
Fever up to 105°F
Myalgia and arthralgia
Nausea and emesis
Pain in the bite site
Rash and ulceration
Skin necrosis
Disseminated intravascular coagulation
tain. Cacy and Mold35 have noted that most brown
recluse bites are clinically insignificant.
Systemic symptoms (Table 1) of loxoscelism can
include fever up to 105° F36 chills, nausea, arthritic
complaints, and blood abnonnalities. 37- 39 Young40
reported the interesting case of a 38-year-old man
who was bitten by a brown recluse spider and who
developed marked thrombocytopenia (platelet
count of 13,OOO/f.l.L) but no associated hemolysis or
disseminated intravascular coagulation. Although
the patient had a few petechiae on his lower extremities, his thrombocytopenia subsequently resolved without sequelae. Several authors have also
described a generalized erythema or scarlatinifonn
rash. 41 - 43 This rash is generally much more severe
in more severely envenomated patients.
Patients with small faciallesions44 secondary to
brown recluse spider bites have had massive facial
edema. Gotto and coUeagues45 described a case of
severe cervical soft-tissue edema and swelling in a
7-year-old boy as a complication of brown recluse
spider bite to the neck. L arizonica envenomation
has been implicated in the induction of shock in a
13-year-old girl in Arizona. lO This patient also developed a dysesthetic, hyperesthetic, sunburn-like
rash on her trunk and proximal extremities. Sauer46
reported the case of a patient who developed bowel
and bladder incontinence, transverse myelitis, and
paralysis after a brown recluse spider bite to the
right buttock. At discharge, nearly 7 112 weeks
later, the patient had recovered only partial use of
his lower extremities.
Within 24 hours after the bite, the local area
around the bite site generally turns a reddish blue
color. A blister or bleb then fonns, and as necrosis
continues, the lesion can evolve into an eschar
during the next 2 or 3 days. The eschar will even-
Table 2. Treatment Regimens for Brown Recluse
Spider Bites.
Early and late sllrgical excision of wound
Wound curettage
Hyperbaric oxygen
tuaIly slough off leaving a crater of variable size but
generally 1 to 2 cm wide. Ulcers can become extensive and enlarge to 30 cm in diameter. Large
ulcers might require up to 6 months to heal completely and could require skin grafting. Some patients will develop persistent, granulating ulcers at
or near the bite site. 36 Recurrent ulcers resembling
pyoderma gangrenosum can develop years later,
even in cases that had originally required treatment
with skin grafts.
Grouping the various clinical symptoms of loxoscelism and necrotic arachnidism by severity of
systemic symptoms can facilitate treatment. 47 Such
grouping is similar to the grading commonly used
when determining the severity of poisonous snake
bites. Patients who experience local bite site pruritus and who lack systemic symptoms are in group 1.
Group 2 comprises patients whose bites exhibit an
area of necrosis approximately 1 cm or less. The
area of necrosis surrounds a central vesicle. Group
3 comprises patients who exhibit' definite systemic
symptoms and who possess ulcers larger than 1 cm.
Group 4 comprises patients who exhibit large ulcers, greater than 4 cm, and who also exhibit severe
systemic symptoms. The usefulness of such grading
schemes in determining severity of envenomation
by fiddleback spiders is questionable because there
is little correlation between the severity of skin
necrosis and the development of systemic symptoms.
The appropriate treatment of brown recluse spider
bites remains controversial, and various treatment
regimens (Table 2) have been advocated with varying success. The care of mild, nonprogressive cases
of brown spider bite, however, should include thorough cleansing of the wound site, elevation of the
bitten extremity, administration of analgesics, and
administration of tetanus vaccine, when indicated.
Patients should be observed closely to see whether
they develop systemic symptoms, at which point
immediate hospitalization is indicated.
Surgical correction of venom-induced skin necrosis can add considerable cost to the treatment of
violin spider bites. Additionally, it is difficult to
determine presumptively which skin lesions will
progress to the point where they will require a
surgical correction. Hershey and Aulenbacher48 advocated treatment with a combination of steroids,
antibiotics, and surgery, where indicated. They admitted that none of these three therapies could
prevent necrosis of the bite site but suggested that
early surgery to remove the involved skin and underlying fat was the preferred therapy. Amold 49
promoted surgical excision of all lesions 1 cm or
greater in diameter. Anderson20 described lesions
that enlarged rapidly. These lesions were reported
to cease enlarging suddenly, at which point they
developed a well-defined margin.
When surgery is performed, it should be done
for lesions that have stabilized, ie, late lesions. The
surgeon must be reasonably confident that no postsurgical enlargement of the lesion will occur. De· et a,I so·III a retrospective study of 31 patients
with hand or upper extremity spider bites, determined that delayed excision of the necrotic lesion
was preferable. He found that as many as 20% of
the patients who underwent early excision of their
necrotic lesions subsequendy developed either a
wound breakdown or a functional limitation in the
use of the bitten extremity. Hollabaugh and Fernandes 44 recommended curettage of the necrotic
tissue with local anesthesia for treatment of brown
spider bites. All 18 of the patients in their study
who were treated with curettage had wounds that
healed without requiring skin grafting. Gutowicz et
al 9 advocated wide excision of the necrotic lesion
after the area of necrosis became well demarcated,
6 to 8 weeks after the bite. Wright et al,51 in a study
of 111 patients with suspected brown recluse spider
bite, found that most did not need surgery; however, 16 of the 111 patients in their study developed
systemic symptoms. Three patients required delayed skin grafting. Two of the 3 patients requiring
skin grafting had initially received dapsone therapy
for treatment of their spider bite.
Jansen et al,52 working with white rabbits, did
not find any treatment value of either intramuscular or intralesional administration of methylprednisolone (Depo-Medrol) in the prevention of dermonecrosis. Berger et al 19 also concluded that large
Brown Recluse Spider Bites 419
doses of steroids had little effect on the progression
or development of necrotic arachnidism. Sauer,46
however, advocated both intramuscular and intralesional injection of cortisone in the treatment of
severe bites.
Anderson 2o advocated the use of steroids only in
severe bites, bites that were associated with loxoscelism, and bites involving small children. For children he specifically recommended using 100 mg of
prednisone daily for a minimum of 3 days, pending
the results of additional studies to rule out hemolysis and renal failure. In this same publication,
Anderson described the development of hemolysis,
intravascular hemorrhage, coagulation, hyponatremia, myoglobinuria, hemoglobinuria, and coma in
a 5-year-old boy who was bitten on his thigh. Steroid therapy was instituted; however, the patient's
decreasing kidney output required peritoneal dialysis. Complete resolution of the sequelae of the
spider bite required a full 12 months.
Dapsone has been a cornerstone of the therapy
of brown recluse spider bite but has severe side
effects. Dapsone has been used to treat brown spider bites because it can inhibit polymorphonuclear
leukocyte diapedesis and infiltration into the bite
site. Animal studies using dapsone have also had
conflicting results. Several authors using venominjected animal models have shown a decrease in
the average size of necrotic lesions in the animals
treated with dapsone. B ,54 Rees et al 36 in a comparative study found that the combination of dapsone
and delayed surgical excision was preferable to immediate surgical resection for the treatment of spider bite. Beilman et al 55 indicated that dapsone, to
be effective, must be administered within 36 hours
of the bite. This study showed no benefit to pretreatment of spider bites with dapsone. This study
also showed no discernible benefit in giving patients dapsone when they sought treatment more
than 36 hours after the bite. Phillips et al,56 however, were unable to detect any clinical benefit
when using dapsone for the treatment of spider
There are serious side effects associated with the
use of dapsone. Almost all patients given dapsone
will develop dose-related hemolysis. Agranulocytosis, aplastic anemias, and methemoglobinemia occasionally occur. Methemoglobin is unable to bind
oxygen and is produced when more than 1% of the
hemoglobin is oxidized to the ferric (HbFe3+)
state. The resulting increase in oxygen affinity of
420 JABFP November-December 2000 Vol. 13 No. 6
oxyhemoglobin shifts the oxyhemoglobin dissociation curve to the left. Methemoglobin levels of
35% or more can produce shortness of breath,
headache, and fatigue. Levels as high as 70% can
result in death of the patient. Patients suffering
from methemoglobinemia usually have a bluish tint
to their mucus membranes and their nail beds.
Peripheral neuropathies, although rare, can also
occur as a consequence of dapsone administration.
Willie and Morrow 57 described a patient who developed fever, chills, nausea, headache, myalgia,
anorexia, and mild hemoglobinuria after treatment
of brown spider bite with dapsone. Dapsone hypersensitivity normally occurs within 6 weeks of starting the drug and resolves within 2 weeks of discontinuing therapy. This syndrome does not appear to
be dose related.
Other commonly seen side effects of dapsone
therapy include sore throat, pallor, purpura, cholestatic jaundice, and hyperbilirubinemia. Many of
these symptoms can also be a result of brown spider
envenomation, thereby confusing the clinical picture. Because of these serious side effects, dapsone
should be reserved for adult patients who have
rapidly progressing, necrotic lesions. It should not
be administered to children. Adults who are selected to receive dapsone must first be screened for
glucose-6-phosphate dehydrogenase deficiency.
Dapsone should be given at dosages of 50 to 100
mg daily.53,58
The effect of hyperbaric oxygen in decreasing
the size of necrotic skin lesions resulting from
brown recluse envenomation has also been studied.
One studl 9 using white rabbits showed an earlier
reepithelization of the necrotic ulcers when these
rabbits were treated with hyperbaric oxygen twice
daily. Treatments were initiated at 72 hours after
injection of venom. Maynor et al 60 speculated that
hyperbaric oxygen inactivated sphingomyelinase D
by the disruption of sulfhydryl groups. Hyperbaric
oxygen has also been postulated to decrease wound
damage secondary to brown recluse envenomation
in at least two additional ways.56 It has been speculated that wound damage is decreased in part
because of the pulmonary sequestration of neutrophils. Hyperbaric oxygen therapy also increases the
production of collagen by fibroblasts, thereby facilitating wound healing. Beilman et al 55 found that
guinea pig models which had hyperbaric oxygen
therapy as pretreatment had significantly smaller
areas of necrosis when compared with control an-
imals or animals given dapsone as pretreatment.
Animals that had hyperbaric oxygen therapy after
the injection of recluse venom did not show a
corresponding decrease in skin necrosis. Phillips et
al,56 however, using white rabbits, were unable to
show any decrease in lesion size when compared
with controls. These animals were injected with 20
f.Lg of L laeta venom and underwent hyperbaric
oxygen therapy 4 hours after the injection. In a
similar manner, Phillips and colleagues were also
unable to show any benefit from treatment with
cyproheptadine or dapsone.
Electric shock therapy has also received attention as a possible mechanism of inactivating the
enzymes contained in brown recluse venom. 54 As
with snake envenomation, using electric shock to
treat spider envenomation is disappointing and
cannot be recommended.
Burton61 described his 10 years of experience
with applying nitroglycerin patches to the bite site
area. His experiences indicate that necrosis and
ulceration can be aborted if the nitroglycerin patch
is applied within 48 hours of the time the patient
was bitten. He promoted the use of a O.l-mgJh
patch and speculated that the nitroglycerin patches
prevented necrosis through reversal of blood vessel
Brown recluse specific antivenin has been shown
by Rees et aj31 to be most effective for limiting
dermonecrosis secondary to brown recluse venom.
Similar to antivenin use in the treatment of poisonous snakebite, brown recluse spider antivenin must
be administered within the first 24 hours. It is most
effective when administered as soon as possible
after the bite, unfortunately at a time when the
amount of venom injected by the spider is open to
speculation. Consequently, it can only be guessed
whether the patient received a sufficient quantity of
venom to require treatment with antivenin.
Insecticides that are effective in reducing brown
recluse sp~der populations have been shown to be
exceedingly toxic to human beings, and their use in
human dwellings is ill advised. Reinfestation is a
continuous problem, and spiders can hide in areas
where insecticides cannot be placed. 59 Good
housekeeping is essential in the prevention of infestation, as the elimination of food sources will
decrease infestation. It is also prudent to avoid
wearing clothes that have been strewn on the floor
during the evening.
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In the article "Treatment of AIDS and HIVRelated Conditions: 2000" by Ronald H.
Goldschmidt and Betty J. Dong Am Board
Fam Pract 2000;13:274-98), an incorrect
Web site was listed for the article in the credit
line (p. 274). The article can be found at http://
The authors regret the error.
In a reply to a letter to the editor (Prenatal
Testing and Counseling for Down Syndrome. J Am Board Fam Pract 2000;13:2278), Dr. Cate's first name should have been
spelled Sara. The publisher regrets the error.
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